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      Remote Analgesic Effects Of Conventional Transcutaneous Electrical Nerve Stimulation: A Scientific And Clinical Review With A Focus On Chronic Pain

      1

      Journal of Pain Research

      Dove

      transcutaneous electrical nerve stimulation, TENS, chronic pain, electrode, remote, widespread

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          Abstract

          Background

          Transcutaneous electrical nerve stimulation (TENS) is a safe, noninvasive treatment for chronic pain that can be self-administered. Conventional TENS involves stimulation of peripheral sensory nerves at a strong, non-painful level. Following the original gate-control theory of pain, stimulation is typically near the target pain. As another option, remote stimulation may also be effective and offers potential advantages.

          Objective

          This narrative review examines mechanisms underlying the remote analgesic effects of conventional TENS and appraises the clinical evidence.

          Methods

          A literature search for English-language articles was performed on PubMed. Keywords included terms related to the location of TENS . Citations from primary references and textbooks were examined for additional articles.

          Results

          Over 30 studies reported remote analgesic effects of conventional TENS. The evidence included studies using animal models of pain, experimental pain in humans, and clinical studies in subjects with chronic pain. Three types of remote analgesia were identified: at the contralateral homologous site, at sites distant from stimulation but innervated by overlapping spinal segments, and at unrelated extrasegmental sites.

          Conclusion

          There is scientific and clinical evidence that conventional TENS has remote analgesic effects. This may occur through modulation of pain processing at the level of the dorsal horn, in brainstem centers mediating descending inhibition, and within the pain matrix. A broadening of perspectives on how conventional TENS produces analgesia may encourage researchers, clinicians, and medical-device manufacturers to develop novel ways of using this safe, cost-effective neuromodulation technique for chronic pain.

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          Most cited references 146

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          Descending pain modulation and chronification of pain.

          Chronic pain is an important public health problem that negatively impacts quality of life of affected individuals and exacts an enormous socio-economic cost. Currently available therapeutics provide inadequate management of pain in many patients. Acute pain states generally resolve in most patients. However, for reasons that are poorly understood, in some individuals, acute pain can transform to a chronic state. Our understanding of the risk factors that underlie the development of chronic pain is limited. Recent studies have suggested an important contribution of dysfunction in descending pain modulatory circuits to pain 'chronification'. Human studies provide insights into possible endogenous and exogenous factors that may promote the conversion of pain into a chronic condition. Descending pain modulatory systems have been studied and characterized in animal models. Human brain imaging techniques, deep brain stimulation and the mechanisms of action of drugs that are effective in the treatment of pain confirm the clinical relevance of top-down pain modulatory circuits. Growing evidence supports the concept that chronic pain is associated with a dysregulation in descending pain modulation. Disruption of the balance of descending modulatory circuits to favour facilitation may promote and maintain chronic pain. Recent findings suggest that diminished descending inhibition is likely to be an important element in determining whether pain may become chronic. This view is consistent with the clinical success of drugs that enhance spinal noradrenergic activity, such as serotonin/norepinephrine reuptake inhibitors (SNRIs), in the treatment of chronic pain states. Consistent with this concept, a robust descending inhibitory system may be normally engaged to protect against the development of chronic pain. Imaging studies show that higher cortical and subcortical centres that govern emotional, motivational and cognitive processes communicate directly with descending pain modulatory circuits providing a mechanistic basis to explain how exogenous factors can influence the expression of chronic pain in a susceptible individual. Preclinical studies coupled with clinical pharmacologic and neuroimaging investigations have advanced our understanding of brain circuits that modulate pain. Descending pain facilitatory and inhibitory circuits arising ultimately in the brainstem provide mechanisms that can be engaged to promote or protect against pain 'chronification'. These systems interact with higher centres, thus providing a means through which exogenous factors can influence the risk of pain chronification. A greater understanding of the role of descending pain modulation can lead to novel therapeutic directions aimed at normalizing aberrant processes that can lead to chronic pain.
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            Spinal cord mechanisms of pain.

            The spinal cord is the first relay site in the transmission of nociceptive information from the periphery to the brain. Sensory signals are transmitted from the periphery by primary afferent fibres into the dorsal horn of the spinal cord, where these afferents synapse with intrinsic spinal dorsal horn neurones. Spinal projection neurones then convey this information to higher centres in the brain, where non-noxious and noxious signals can be perceived. During nociceptive transmission, the output of the spinal cord is dependent on various spinal mechanisms which can either increase or decrease the activity of dorsal horn neurones. Such mechanisms include local excitatory and inhibitory interneurones, N-methyl-D-aspartate receptor activation, and descending influences from the brainstem, which can be both inhibitory and excitatory in nature. After nerve injury or conditions of inflammation, shifts can occur in these excitatory and inhibitory mechanisms which modulate spinal excitability, often resulting in the heightened response of dorsal neurones to incoming afferent signals, and increased output to the brain, a phenomenon known as central sensitization. In this review, we consider the ways in which spinal cord activity may be altered in chronic pain states. In addition, we discuss the spinal mechanisms which are targeted by current analgesics used in the management of chronic pain.
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              Temporary abolition of pain in man.

               P. Wall,  D Sweet (1967)
              In eight patients with intense chronic cutaneous pain, sensory nerves or roots. supplying the painful area were stimulated. Square-wave 0.1-millisecond pulses at 100 cycles per second were applied, and the voltage was raised until the patient reported tingling in the area. During this stimulation, pressure on previously sensitive areas failed to evoke pain. Four patients, who had diseases of their peripheral nerves, experienced relief of their pain for more than half an hour after stimulation for 2 minutes.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                JPR
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                26 November 2019
                2019
                : 12
                : 3185-3201
                Affiliations
                [1 ]NeuroMetrix , Waltham, MA, USA
                Author notes
                Correspondence: Shai N Gozani NeuroMetrix , 1000 Winter Street, Waltham, MA 02451, USATel +1 781 314 2789Fax +1 781 890 1556 Email gozani@neurometrix.com
                Article
                226600
                10.2147/JPR.S226600
                6885653
                © 2019 Gozani.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Tables: 3, References: 185, Pages: 17
                Categories
                Review

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